Individuals with neurodegenerative diseases demonstrate upper airway deficits that are primarily due to loss of hypoglossal lower motor neurons (XII LMNs). These deficits lead to aspiration pneumonia and death; however, there are no treatments available to consistently and significantly improve upper airway function. Tongue exercise mitigates upper airway deficits in a rat model of XII LMN death (intralingual injection of cholera toxin B conjugated to saporin; CTB-SAP), but the mechanism responsible for this alleviation is unknown. Our pilot data suggests that tongue exercise upregulates XII expression of brain derived neurotrophic factor (BDNF) in CTB-SAP rats, and that tongue exercise-induced improvement of upper airway function is lost following inhibition of tropomyosin receptor kinase B (TrkB; the high-affinity receptor for BDNF). However, XII TrkB expression +/- tongue exercise in CTB-SAP rats is undetermined. We hypothesize that decreased XII TrkB expression in CTB-SAP rats will be upregulated back towards control levels with tongue exercise. To study XII TrkB expression, we first conducted immunohistochemistry with TrkB and CTB antibodies on perfused brainstem tissue from control and CTB-SAP rats +/- tongue exercise (n=8/group). Confocal microscopy and subsequent ImageJ analysis is currently underway to quantify XII TrkB expression. Our preliminary data suggest XII TrkB expression in CTB-SAP + tongue exercise rats is similar to control rats but is increased vs. CTB-SAP + sham exercise rats, providing further evidence of the BDNF pathway underlying tongue exercise-induced changes following XII LMN loss. Lastly, these results would suggest that the BDNF pathway could be a target for treatment for upper airway deficits in individuals with neurodegenerative diseases. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
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